Physiotherapy treatment of Bell’s Palsy: A case report Case Report

Case Report
Physiotherapy treatment of Bell’s Palsy: A case report
James M. Elliott a,b, c
Rueckert-Hartman School for Health Professions,
Department of Physical Therapy, Regis University, Denver, Colorado, USA
b
Division of Physiotherapy, School of Health and Rehabilitation Sciences,
The University of Queensland, Brisbane, Australia
c
Sport and Spine Physical Therapy, Centennial, Colorado, USA
a
ABSTRACT
Facial nerve (Cranial Nerve VII) paralysis can be a disguring disorder with profound
physical and social impact upon the patient. A common diagnosis related to facial
nerve paralysis is Bell’s palsy. The aetiology of Bell’s palsy is largely unknown, although
it may be congenital, iatrogenic, or result from neoplasm, infection, neurovascular
insult, trauma, or toxic exposure. Symptoms may include paresis, hyperacusis,
decreased production of tears, altered taste, otalgia, aural pressure and facial
pain. Although recovery is expected without intervention in most cases, incomplete
recovery is not infrequent. This case report describes a physiotherapy treatment
based on current best evidence for a patient with left facial nerve paralysis. The
patient was a 53-year-old Caucasian male with complete left-facial paralysis with
a diagnosis of Bell’s palsy. Signs and symptoms were assessed using a standardized
measure of facial disability (Facial Disability Index-FDI). Physiotherapy rehabilitation
involved muscle-re-education exercises aimed at restoring normal movement within
the affected left facial musculature. In 16 physiotherapy sessions over 4 months,
the patient had improved self-reported facial disability (initial FDI score; Physical
subscale = 35/100 and Social/Well-being subscale = 55/100. The nal FDI score;
Physical subscale = 75/100 and Social/Well-being subscale = 85/100) and signicantly
reduced functional impairments.
Generally, patients diagnosed with Bell’s palsy may expect complete recovery
without medical and/or physiotherapy intervention. However, some cases remain
complicated without complete resolution of symptoms. The need to accurately
classify these patients exists. In some cases, physiotherapy may provide extreme
benet in reducing the physical and social impairments commonly observed in
patients suffering from Bell’s palsy. Self-reported outcome measures, such as the
FDI, provide an easy method to assess whether patients suffering from various
diagnoses are responding to physiotherapy. The use of such outcome measures
will also provide objective evidence of efcacy for third-party payers. Elliott JM
(2006): Physiotherapy treatment of Bell’s Palsy: A case report. New Zealand Journal
of Physiotherapy 34(3): 167-171.
Key Words: Bell palsy, Physiotherapy, Rehabilitation
INTRODUCTION
Bell’s palsy is a complex neuromuscular facial
disorder of unknown aetiology commonly affecting
the motor neurones of facial muscles receiving
their neurological innervations from the seventh
cranial nerve (the facial nerve) (VanSwearingen
and Brach, 1998). Most patients’ symptoms
spontaneously resolve; however some patients
continue to suffer in the long-term. Indicators for
poor prognosis include complete facial palsy, no
recovery of symptoms by three weeks, age over 60
years, severe pain, herpes zoster virus, co-morbid
status e.g. hypertension, diabetes, pregnancy and
severe degeneration of the facial nerve shown by
electrophysiological testing (Holland and Weiner,
2006). Ultimately, the signs and symptoms related
to long-term Bell’s palsy may have a negative effect
on many aspects of an individual’s lifestyle. From
a functional perspective, the ability to drink, eat
and express oneself (verbally/non-verbally) can
be greatly disturbed. In addition, the psychosocial
impact of such a disorder can be life-altering in
relation to social functioning. Treatment often
NZ Journal of Physiotherapy – November 2006, Vol. 34 (3)
consists of a dose trial of antibiotics, antiviral
or anti-inammatory agents and in some cases,
surgical decompressive procedures at the facial
nerve exit zone (stylomastoid foramen) may be
considered (Holland and Weiner, 2006). Further
to these medical options for the treatment of Bell’s
palsy, physiotherapy has been reported to improve
the impairments associated with facial paralysis
(Brudny et al., 1988; Brudny et al., 1991; Ross et
al., 1991; Brach et al., 1997; VanSwearingen and
Brach, 1998; Beurskens and Heymans, 2003).
The purpose of this case report is to describe
current best evidence conservative rehabilitation
approach using a facial neuromuscular reeducation scheme for an individual diagnosed with
Bell’s palsy
CASE DESCRIPTION
The patient (“MG”) was a 53-year-old Caucasian
male diagnosed with Bell’s palsy of the left facial
nerve with severe left facial paralysis. The initial
physiotherapy evaluation was conducted 6 weeks
following the onset of symptoms of left facial
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paralysis. At the time of the initial physiotherapy
evaluation, the patient did not report any other
signicant medical problems with the exception
of his status as a non-insulin dependent diabetic
(NIDDM). He managed his NIDDM status with
diet and exercise. MG reported that his left facial
symptoms came on suddenly with mild pain,
markedly decreased sensation in the left face,
decreased production of tears but without otalgia,
altered taste, hyperacusis or aural fullness. He
denied ever having suffered any neck pain nor
could he recount any previous trauma to his
cervical spine. However, he did report insidious
long-standing symptoms (~ 20 years) of hearing loss
in his left ear accompanied by vague, infrequent
bouts of dizziness/unsteadiness of unknown origin.
Further questioning aimed at uncovering other
precipitating factors or prodromal symptoms related
to his dizziness/unsteadiness was unremarkable.
He was initially examined by his family physician
who prescribed a course of anti-viral (acyclovir)
medication, oral steroids (prednisone) and ordered
a magnetic resonance imaging study of his head
and cervical spine. No imaging abnormalities
were discovered. No electrophysiological nerve
conduction studies were ordered or performed e.g.
blink reex study. He continued to take prednisone
at the time of the initial physiotherapy evaluation
but the acyclovir medication was discontinued
due to lack of response in relation to his facial
symptoms.
There were no reports of an acute change for
his left sided hearing loss accompanying his facial
paralysis; however, he did report reduced tear
production and sensation loss in the left side of his
face. The physiotherapy evaluation further consisted
of a qualitative analysis of his resting facial posture
and neurological examination of the head and
face, which revealed hypo-esthetic response to
pinwheel testing in the three terminal branches
of the left trigeminal nerve ((V1) ophthalmic, (V2)
maxillary and (V3) mandibular). MG’s resting
facial posture revealed severe asymmetry with a
left sided droop. Voluntary movement of the leftsided facial musculature was barely visible whereas
the uninvolved right-sided facial musculature
was clearly intact. The physiotherapist (JE)
also performed active
and passive cervical
movements with no
significant findings in
relation to the patient’s
facial symptoms or
aberrant movements.
To assess self-reported
disability at baseline and
to monitor treatment progress, the patient completed
the Facial Disability Index (FDI), developed by
VanSwearingen and Brach (1996). The FDI is a tenitem questionnaire used for assessing the disability
of patients with facial nerve disorder. The FDI is
designed to provide the clinician with information
regarding the disability as well as related social
and emotional well-being of the patient. The FDI
consists of two subscales; Physical function (items
1-5) and social well-being (items 6-10). The scores
range from 0 (complete paralysis) to 100 (normal
facial function). The FDI has shown to be reliable
and valid as a clinical instrument and has been
shown to accurately demonstrate the relationship
between impairments, disability, and psychosocial
status (VanSwearingen and Brach, 1996). MG’s
initial FDI score on initial evaluation was; Physical
function subscale = 35/100; Social/Well-being
subscale = 55/100.
MG was a full-time truck driver for a local
moving company. His duties required him to be
on the road for 12 hour shifts, twice per week. He
lived alone and reported signicant difculty with
drinking, eating, speaking and closing his left eye.
These functional impairments were consistent
with examination ndings of synkinesis (abnormal
movement of the face during a desired motion) for
his left and right-sided muscles of facial expression
e.g. smiling, ‘puckering’ and frowning. MG also
remarked on the need to continually use eye drops
as well as performing manual closure of his left eyelid in order to relieve the symptoms of a dry, irritated
left eye. These symptoms were consistent with the
clinical presence of a positive Bell reex on the left
side (eye rolling backward during active eye closure)
which prevented complete eye closure (Jelks et al.,
1979). He appeared motivated to improve his facial
function with physiotherapy intervention.
It was initially decided that the patient would
be seen one time per week for up to 12 weeks,
with each session scheduled for 45 minutes. Each
session began with a brief re-evaluation of facial
motor functioning e.g. active smiling, frowning,
‘puckering’ and eye closure.
TREATMENT
It was evident that the patient’s goals were
to improve his facial functioning as well as
decrease his concern for an impaired aesthetic
appearance. In order to assist MG achieve his
goals, the treating physiotherapist (JE) performed
a literature review on current best evidence for
Bell’s palsy and physiotherapy treatment. The
literature review yielded
recommended guidelines
described by Brach and
VanSwearingen (1999).
The authors describe four
distinct treatment based
categories (initiation,
facilitation, movement
control and relaxation
stages) matched with specic treatment techniques
for each category. These categories can provide
helpful guidelines for treatment planning and
progression (Brach and VanSwearingen, 1999).
Based on the findings of his initial clinical
assessment, MG tted within the initiation phase
“four distinct treatment-based
categories … provide helpful
guidelines for treatment planning
and progression”
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NZ Journal of Physiotherapy – November 2006, Vol. 34 (3)
of treatment according to the system devised by
Brach and VanSwearingen (1999). Therefore, the
exercises consisted of actively assisting specic
facial movements. In particular, MG was instructed
on using his ngers to passively move the left
corner of his mouth into a ‘smiling’ posture. He was
informed to then slowly release his nger pressure,
all the while attempting to actively hold the ‘smiling’
posture with the involved musculature. In addition
to the ‘smiling’ exercise, MG was instructed to
passively raise his left eyebrow with his nger and
activate the appropriate musculature upon release
of his passive support nger.
BIOFEEDBACK
Surface EMG (s-EMG) has been advocated as
an appropriate form of visual and/or auditory biofeedback for the re-education of muscle activity in
facial movement disorders. However, if s-EMG is not
available, a hand mirror may be substituted in order
provide visual feedback during the performance of
exercises (Brach and VanSwearingen, 1999). As sEMG was not available in our clinic, the patient was
informed to utilize a hand-held mirror during the
performance of his exercises in order to decrease,
if not eliminate, unwanted synkinesis.
During this initiation phase, MG was instructed
to perform these facial exercises with 5-10
repetitions at a frequency of 3-5 times per day.
MG was provided explicit instructions to cease
performance of the exercises if fatigue set in and/
or the exercises could not be performed without
synkinesis. Our primary goal was to initiate the
activation of his left-sided musculature and to
reduce, if not eliminate, the poor mass synkinesis
patterns which were initially present.
The patient, intrigued by this approach, began
his exercises at somewhat of a ‘feverish’ pace and
was informed on treatment number 2 to reduce the
effort put forth as he was likely only contributing to
a faulty motor control program e.g. over-facilitating
the uninvolved right-side. As a result, treatment,
at least for the rst ve treatments, consisted of
manually ‘walking’ the patient through what was
believed to be ‘just enough’ vs. ‘too much’ effort with
the initiation exercises. The other issue that the
patient had to contend
with was the quick
onset of muscular
fatigue on the left side,
likely due to the highload effort put forth
initially. When fatigue occurred, the patient was
instructed to cease performance of the exercises
and then commence later in his day.
As previously stated, MG also complained of a
dry, irritated left eye and this was accompanied
with a positive Bell reex on the left side. The
physiotherapist decided to introduce the exercise
put forth by VanSwearingen and Brach (1999) in
which the patient is instructed to focus both eyes
on an object (e.g. the tip of a nger) positioned
down and in front of the patient. Once the
patient identies the target, he/she should then
attempt to close his/her eyes. The patient should
ultimately work towards complete eye closure and
it is suggested that having the patient focus on
a downward target/object may help initiate the
closure of the involved upper eyelid.
For MG, this approach appeared to counteract
the positive Bell reex. Once he was able to actively
close his left eye in a consistent manner, the
target was moved in a horizontal direction while
his eyes were closed. Upon eye-opening, MG was
instructed to keep his head still and actively track
and locate the object and then repeat the eye-lid
closure exercise. This also became part of his home
exercise repertoire; 5-10 repetitions of eye closures,
3-5 times per day.
Following the 5 th visit, MG’s neurological
exam began to change in that he demonstrated
symmetrical sensation with pinwheel testing in
the (V3) mandibular division of the trigeminal
nerve. The return of sensation to the lower third
of the face was also accompanied by an increased
ability to develop trace activity in the upper left
lip corner with active smiling. Sensation remained
unchanged in the left (V1) opthalmic and (V2)
maxillary divisions of the trigeminal nerve. The loss
of sensation to the upper part of the face remained
asymmetrical until the 10th visit, whereupon the
exam ndings revealed improved, although slightly
diminished, sensation throughout the left V1 and
V2 distributions. V3 remained symmetrical.
Re-evaluation on the 10th treatment session
revealed that MG was beginning to demonstrate
improved resting facial posture and active initiation
of the involved left sided musculature. As a result,
it was decided to progress the patient to the next
category of treatment; the facilitation stage. It was
also decided that the patient would be seen every
other week secondary to his demanding job hours
and apparent independence with both the activeassisted and eye-closure exercises and reduced
signs of synkinesis.
In keeping with the guidelines put forth by Brach
and VanSwearingen (1999), resistive exercises
were introduced and aimed at facilitating the
left-sided musculature.
Specifically, MG was
instructed on how to
use his nger to provide
resistance to the desired
facial movements e.g.
smiling, ‘puckering’ and raising his eyebrow on the
left side. Once again, careful attention was taken to
avoid muscular fatigue of the involved side and overfacilitation of the uninvolved side. MG was instructed
to increase the number of repetitions to 20 and to
perform the exercises (1-2 times per day) once in the
morning and once before going to bed at night. He
continued this regime over the next two months.
On the 16th and nal visit, MG demonstrated
complete independence with his facilitation
“avoid muscular fatigue of the
involved side and over-facilitation of
the uninvolved side”
NZ Journal of Physiotherapy – November 2006, Vol. 34 (3)
169
a)
b)
170
a)
b)
Figure 1. Qualitative images of resting facial posture a)
October, 2005 and b) February, 2006
Figure 2. Qualitative images of active smile a) October,
2005 and b) February, 2006
exercises. This was consistent with marked
improvement in his resting facial posture and
active control of specic facial movements e.g.
smiling, raising his left eyebrow without synkinesis
and complete left eyelid closure. MG was asked
to complete the FDI once more. This indicated
improvement in both the physical function subscale
= 75/100 (from 35/100 at baseline) and the social/
well-being subscale = 85/100 (from 55/100 at
baseline). MG’s improved scores were accompanied
with self-reports of signicant improvement with
drinking, eating, speaking and closing his left eye.
Based on these signs and symptoms, improved FDI
scores and his reports of satisfaction in relation
to his perceived aesthetic appearance (see Figs. 1
and 2), MG was discharged from physiotherapy
following 16 total visits spread over 4 months.
Despite not progressing to the movement control
category, MG demonstrated signicant functional
improvement in his left facial Bell’s palsy. He vowed
to continue with his exercises as he felt that they
may be required to prevent further problems related
to symptoms of facial paralysis.
DISCUSSION
Features of successful outcomes for patients
suffering from Bell’s palsy are likely to be reliant
on accurate diagnoses and appropriate followup with a team-oriented approach. Delivery of
conservative, categorical physiotherapy care
has provided evidence for successful outcome in
some cases of patients with Bell Palsy (Brach and
VanSwearingen, 1999; Beurskens and Heyman,
2003). In some cases, additional pre-testing may
be of value in determining the aetiological features
leading to the accurate diagnosis. For example
electrophysiological nerve conduction study of the
blink reex in patients with Bell’s palsy usually
demonstrates prolonged latencies and/or absent
early and late responses to stimulation (Kimura
et al., 1976; Leon-Sarmiento, 2002). Although a
blink reex study was not initially performed on
NZ Journal of Physiotherapy – November 2006, Vol. 34 (3)
this particular patient, the results of such a test
would yield objective evidence of the physiological
status of the facial nerve. This may then provide
some prognostic information and allow for early
and appropriate classication of patients with
symptoms of facial paralysis.
While unknown, it may be that MG’s insidious
onset of Bell’s palsy is related to his past medical
history, including hearing impairments and vague
bouts of dizziness/unsteadiness. The seventh and
eighth cranial nerves (facial and vestibulocochlear)
consistently course towards the internal auditory
canal within the cerebellopontine angle (Haines,
2006). Lesions, such as contact compression of
the seventh and eighth cranial nerves with the
neurovascular loop formed by the anterior inferior
cerebellar artery, in this anatomical region are not
uncommon (Maurer et al., 2000). The resultant
symptoms may include unilateral sensorineural
hearing loss, tinnitus, vestibular disorders and
hemifacial symptoms (Gierek et al., (2000). This
particular patient does have a long-standing history
of otologic impairment (hearing loss in the left ear and
vague complaints of dizziness/unsteadiness). The
clinical question may then become whether or not
his history of hearing impairments and dizziness/
unsteadiness are related to vascular compression
of the cranial nerves at the cerebellopontine
angle. Therefore, it is reasonable to speculate as
to whether or not MG’s insidious onset of Bell’s
palsy may have been reective of neurovascular
compression of the seventh and eighth cranial
nerves at the cerebellopontine angle? In addition,
the question then arises as to whether this patient is
at risk for recurrence of his Bell’s palsy symptoms?
Finally, it could be argued that a collection of these
symptoms should warrant further medical work-up
for abnormalities within the vascular loop before a
denitive diagnosis can be made.
It should also be stated that there is no assumption
being made that this particular patient’s successful
outcome was solely related to the neuro-muscular
re-education scheme. As with many physiotherapy
interventions, it can and must be asked whether or
not the patient got better because of our intervention
or in spite of it? However, this particular patient
had suffered from the related symptoms of Bell’s
palsy for up to six weeks prior to commencing
physiotherapy treatment. Successful resolution
of his symptoms was not achieved over that time
with traditional medical intervention (anti-viral and
anti-inammatory medications). This exceptional
patient was extremely motivated and compliant with
his physiotherapy exercise program. Therefore, it
is believed that along with improved scores on his
FDI, his compliance to the prescribed exercises was
a large factor into his successful outcome.
CONCLUSION
Disorders of the facial nerve, including paralysis,
are not rare and have a variety of potential causes.
The appropriate diagnosis and treatment are very
important to achieving the best possible recovery
NZ Journal of Physiotherapy – November 2006, Vol. 34 (3)
of facial nerve function. Patients suffering from
Bell’s palsy may benet from specic categorical
physiotherapy treatments designed to improve
physical functioning as well as social well-being.
The use of the FDI should be advocated in
determining the efficacy and progression of
physiotherapy treatment of patients with Bell’s
palsy. It also provides objective evidence of
functional improvement; evidence that is often
required by third party payers.
Many clinical presentations have different
etiologies despite symptom similarities, and caution
should be exercised regarding patients having
similar clinical presentations. Further clinical
investigation and research with a larger population
of patients is necessary before a more specic
diagnostic/treatment regimen of this type can be
recommended. In this regard, however, because
of the paucity of available similar documentation
in the professional literature, any comments and
experiences that other clinical providers have
experienced with this type of patient would be
welcomed.
REFERENCES
Beurskens CHG, Heymans PG. Positive effects of mime therapy
on sequelae of facial paralysis: stiffness, lip mobility, and
social and physical aspects of facial disability. Otol Neurol
2003; 24:677-681.
Brach JS, VanSwearingen JM. Physical therapy for facial
paralysis: A tailored treatment approach. Physical Therapy
1999; 79(4): 397-404.
Brach JS, VanSwearingen JM, Lennerrt J, Johnson PC. Facial
neuromuscular retraining for oral synkinesis. Plast Reconstr
Surg 1997; 99: 1922-31.
Brudny J. Biofeedback in facial paralysis: electromyographic
rehabilitation. In: Rubin L, ed. The Paralyzed Face. St. Louis,
MO: Mosby-Year Book; 1991;247-264.
Brudny J, Hammerschlag PE, Cohen NL, Ransehoff J.
Electromyographic rehabilitation of facial function and
introduction of a facial grading scale for hypoglossal-facial
nerve anastomosis. Laryngoscope 1988; 98: 405-10.
Gierek T, Kluczewska E, Pilch J, Zygan L. Vascular compression
syndrome of the vestibulocochlear nerve-otolaryngologic and
radiologic diagnosis. Otolaryngol Pol 2000; 54(6): 763-7.
Holland NJ, Wiener JM. Recent developments in Bell’s Palsy.
BMJ 2006; 329(4): 553-557.
Jelks GW, Smith B, Bosniak S. The evaluation and management
of the eye in facial palsy. Clin Plast Surg. 1979;6:397-419.
Kimura J, Giron LT, Young SM. Electrophysiological study of
Bell palsy: electrically elicited blink reex in assessment of
prognosis. Arch Otolaryngol 1976; 102 (3):104-143.
Leon-Sarmiento FE. Blink reex and discomplete facial nerve
palsy. Arch Med Res 2002;33(1):85-7.
Haines DE (2006): Fundamental neuroscience for basic and
clinical applications (3 rd ed.). Philadelphia: Churchill
Livingstone, pg.169.
Maurer J, Ecke U, Schmidt CL, Stoeter P, Mann W. Vascular
origin of cerebellopontine angle syndrome. HNO 2000; 48(2):
142-6.
Ross B, Nedzelski JM, McLean JA. Efcacy of feedback training
in long-standing facial nerve parresis. Laryngoscope 1991;
101: 744-750.
VanSwearingen JS, Brach JS. The facial disability index: 2.
Reliability and validity of a disability assessment instrument
for disorders of the facial neuromuscular system. Physical
Therapy 1996; 76(12): 1288-1300.
VanSwearingen JS, Brach JS. Validation of a treatment-based
classication system for individuals with facial neuromotor
disorders. Physical Therapy 1998; 78(7): 678-689.
ADDRESS FOR CORRESPONDENCE:
James M. Elliott, 3333 Regis Blvd G-4, Denver CO, 80221,
USA. Phone +1 303-458-4022 Fax +1 303-964-5474. Email: jelltt@
regis.edu
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